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Query: UMLS:C0001511 (Adhesion)
 5,955 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Adhesion molecules expressed on surface membranes of lymphocytes and other leukocytes enable their entry into the lymphoid and other tissues. However, little is known about molecules that govern the transit of leukocytes through the parenchyma of lymphoid organs proper. We show that in comparison to blood leukocytes, the corresponding cells isolated from lymphoid organs, i.e., lymph nodes and spleen, have a significantly augmented expression of certain surface molecules. The helper and cytotoxic subsets of T cells, as well as B cells, display the increased expression of CD44, ICAM-1 and LFA-1, whereas B cells additionally show the augmented expression of MHC class II. In comparison with blood monocytes, splenic monocytes show the increased expression of ICAM-1 and MHC class II molecules. When compared with blood NK cells, splenic NK cells only show the increased expression of ICAM-1. The molecules, which we show to be up regulated upon the entry of leukocytes into lymphoid organs, could be involved in their retention within the tissue via cell-cell or cell-extracellular matrix interactions and in control of their transit through lymphoid tissues.
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PMID:Blood lymphocytes, monocytes and NK cells modulate their expression of CD44, ICAM-1, LFA-1 and MHC class II after arrival into lymphoid organs. 1562 1

Initial adhesive contacts between T lymphocytes and dendritic cells (DCs) facilitate recognition of peptide-MHC complexes by the TCR. In this report, we studied the dynamic behavior of adhesion and Ag receptors on DCs during initial contacts with T-cells. Adhesion molecules LFA-1- and ICAM-1,3-GFP as well as MHC class II-GFP molecules were very rapidly concentrated at the DC contact area. Binding of ICAM-3, and ICAM-1 to a lesser extent, to LFA-1 expressed by mature but not immature DC, induced MHC-II clustering into the immune synapse. Also, ICAM-3 binding to DC induced the activation of the Vav1-Rac1 axis, a regulatory pathway involved in actin cytoskeleton reorganization, which was essential for MHC-II clustering on DCs. Our results support a model in which ICAM-mediated MHC-II clustering on DC constitutes a priming mechanism to enhance antigen presentation to T-cells.
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PMID:Synaptic clusters of MHC class II molecules induced on DCs by adhesion molecule-mediated initial T-cell scanning. 1587 88


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